1. Field of the Invention.
The present invention relates generally to apparatus for intravaginal stimulation for use in the therapy of female urinary incontinence.
2. Description of the Prior Art.
The obstruction of urinary flow in females is managed by various contractive maneuvers of both involuntary smooth muscle and voluntary striated muscle. The first point of resistance is supplied by the so-called internal urethral sphincter. This sphincter is physiologic and consists of a continuation of smooth muscle from the bladder wall. Active contraction of the bladder causes a longitudinal contraction of this muscular layer, thereby shortening the urethral length and widening the urethral lumen. This action constitutes a relaxation of the sphincter. Sympathetic tone inhibits this opening of the internal urethral sphincter. Resistance to urine flow is also to some extent modulated by the tone of the urethral smooth muscle. Contraction decreases the lumenal diameter. This is also mediated by the sympathetic nervous system.
A second point of resistance to the flow of urine is the contracted external urethral sphincter. The external urethral sphincter consists of a circumferental cord of striated muscle and is innervated by the voluntary nervous system via the pudendal nerve. The autonomic reflex pattern, causing bladder emptying, can be inhibited by volitional contraction of the external urethral sphincter.
Alteration of the geometry of the pelvic floor also increases resistance to urine flow. The pelvic floor is created by a sling of striated muscle attached to the pelvic ring. These muscles, like the external urethral sphincter, are under voluntary control. The constituents of the pelvic floor musculature are the deep transverse perineal muscle and the levator ani (pubococcygeus, iliococcygeus) muscles blending with the external anal sphincter. Innervation for all groups derives from the pudendal nerve. Contraction of the pelvic floor musculature elevates the bladder, stretches the urethra, and causes an acute angulation of the urethral-vesicular junction. These alterations in the geometery of the urethra further increase the resistance to the flow of urine.
Urinary incontinence, the inability to control the passage urine, is a relatively common problem in females. Although there are a variety of different types of urinary incontinence, stress incontinence and urge incontinence are the most common. These two forms of incontinence are oftentimes found to exist together, a condition characterized as mixed incontinence.
Stress incontinence is described by the patient as the unacceptable passage of urine under the stress of increased abdominal pressure. This increased pressure typically results from coughing, sneezing, and Valsalva. Stress incontinence is manifest urologically by normal cystometry, obtuse urethral vesicular angle, abnormally low urethral pressures and a physiologically short urethral length. This disorder is most common in multiparous, post-menopausal females. Physiologically, stress incontinence is a disorder of the volitional muscular control of the urethral resistance to the flow of urine. Laxity and partial denervation of the pelvic musculature is the chief abnormality.
Urge incontinence is described as the involuntary passage of urine with a concomittant sense of urgency. Systometry indicates detrusor (bladder wall muscle) contractions with low bladder filling pressures and volumes. These bladder contractions may not be inhibited in the presence of voluntary EMG signals from the sphincter, indicating reduction or loss of the pudendal-parasympathetic inhibitory reflex. Unsolicited, premature bladder contraction may result from mucosal irritation of varied etiology. These premature contractions of the bladder may also be the result of an abnormally high gain in the detruser contractile reflex due to the loss of inhibitory control with an upper-motor-neuron lesion.
Electrical stimulation delivered by an intravaginal or a perineal surface electrode has been shown to inhibit premature and inappropriate detruser contractions. The mechanism for this effect derives from the stimulation of pudendal nerve afferents (sensory receptors or sensory nerve fibers). Input into the pudendal afferent system inhibits a parasympathetic reflex loop consisting of bladder wall afferents (sensory) and efferents (motor). This parasympathetic loop normally senses a distension of the blader via the afferent limb and responds by sending an efferent signal to contract the bladder.
Stimulation of pudendal nerve afferents causes a reflexive contraction of the pelvic floor musculature, mediated by pudendal nerve efferents. In this respect, therapeutic stimulation for stress incontinence requires the same afferent input as that for urge incontinence. However, mobilization of the pelvic floor muscles requires a greater input than that required for bladder relaxation. It is known that the stimulation of the neighboring pelvic floor musculature, such as the deep transverse perineal and external urethral sphincteric muscles, and/or local efferent nerve input, will cause contractions which help prevent incontinence.
Vibratory or other tactile stimulus for stimulating sensory receptors is known generally in neurophysiology. By way of example, sexual aids sometimes include vibratory transducers. However, the use of tactile stimulus for controlling urinary incontinence is apparently undocumented.
It is evident that there is a continuing need for improved urinary incontinence stimulation systems. Although various physiological mechanisms for preventing incontinence are known, they are ineffectively utilized by known stimulation systems. A stimulation system which maximizes the direct motor neural input yet makes use of a variety of physiological sensory reflex mechanisms to prevent incontinence is desired. This system must also be convenient and comfortable to use, to ensure patient acceptance.